Long noncoding RNA SNHG16 promotes human retinoblastoma progression via sponging miR-140-5p

Small nucleolar RNA host gene 16 (SNHG16), a long non-coding RNA, was reported to function as an oncogene in multiple cancers. However, its biological function and regulatory mechanism in retinoblastoma (RB) has not yet been revealed. In this study, we attempted to ascertain the biological role and underlying regulatory mechanism of SNHG16 in RB progression. The expression levels of SNHG16 were measured in RB tissues and cell lines. The effects of SNHG16 knockdown on the proliferation, colony formation, cell cycle progression and apoptosis were investigated using corresponding experiments. Bioinformatic analysis, luciferase reporter assay, and RNA immunoprecipitation assay were applied to identify potential microRNAs (miRs) that could bind with SNHG16. A nude model was established to investigate the effect of SNHG16 knockdown on tumor growth in vivo. We found that SNHG16 expression was upregulated in RB tissues and cell lines compared with normal controls. Knockdown of SNHG16 in RB cells significantly inhibited the proliferation and colony formation, and promoted apoptosis in vitro, as well as retarded tumor growth in vivo. Mechanistic investigation illustrated that SNHG16 acted as a sponge for miR-140-5p and regulated its expression in RB cells. Clinical evidence revealed a negative correlation between SNHG16 and miR-140-5p in RB specimens. Rescue experiments showed that inhibition of miR-140-5p partially attenuated the growth-suppressing effects of SNHG16-depletion on RB cells.. Collectively, SNHG16 exerts oncogenic role in RB by sponging miR-140-5p, suggesting that SNHG16 might be a potential therapy target for RB.